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Objective To investigate the mechanism of action of Huzhang Qingmai decoction (HZQMY) on the improvement of cognitive function in mice with chronic cerebral ischemia from the perspective of intestinal flora. Methods A mouse model of chronic cerebral ischemia was established by placing microcoils around the bilateral common carotid arteries to induce bilateral carotid artery stenosis (BCAS). After 12 weeks of intragastric administration, the cognitive function of the mice was measured by the Morris water maze; the myelin damage was analyzed by LFB staining; The contents of the cecum of the mice in each group were extracted and analyzed by 16S rRNA sequencing. Results The results of the water maze experiment showed that the mice in the HZQMY group had a significantly shorter escape latency, increased the number of crossings platform and the percentage of target quadrants. LFB staining showed that the white matter damage in the model group was severe; the white matter damage in the HZQMY group was milder. The results of 16S rRNA sequencing showed that compared with the model group, the abundance of Verrucomicrobiota, Akkermansia, and ErysiPelatoclostridium capsulatum in the intestinal flora in HZQMY group was significantly reduced (P<0.05), while the abundances of Eubacterium_xylanoPhilum and Allobaculum were significantly increased (P<0.05). Conclusion The protective effect of HZQMY, which has the effect of improving cognitive function in mice with chronic cerebral ischemia, may be related to the regulation of intestinal flora in mice with chronic cerebral ischemia.
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Objective To explore the mechanism of motherwort in the treatment of nerve injury. Methods The active components of motherwort were obtained by searching TCMSP and BATMAN-TCM databases. The action targets of candidate compounds were collected and predicted from TCMSP and SwissTargetPrediction (STP) databases. The target genes corresponding to the active components of motherwort were obtained by using the standardized database of disease targets (Uniprot). The potential targets of motherwort in the treatment of nerve injury were obtained by mapping the disease genes of nerve injury with the three databases of Genecards, DisGenet and OMIM. The network topology analysis software Cytoscape 3.6.0 was used to construct the action target network of motherwort active components. The protein interaction platform database (STRING) was used to construct the interaction relationship between action targets. The target protein interaction (PPI) network was constructed by introducing Cytoscape 3.6.0 software. Through STRING database, GO enrichment analysis and KEGG pathway enrichment analysis were carried out to analyze the target points of motherwort in the treatment of nerve injury. Results 19 active components were screened from motherwort, involving 654 action targets, including 426 action targets related to nerve injury and 6 key targets. These target genes were mainly involved in biological regulation, oxidative stress response and cell communication and other biological processes. Molecular functions were mainly related to protein binding, ion binding and catalytic reduction. They were enriched outside the cell membrane. Its mechanism was related to signal pathways such as MAPK, Toll-like receptor, PI3K-Akt, TNF, IL-17, and apoptosis. Conclusion The active components of motherwort may play a protective role on nerve injury through anti-inflammation, anti-apoptosis and promoting cell growth.
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Innate immunity is the host's first line defense against pathogens invading to the body. Detection of abnormal nucleic acids in the cytoplasm showed that some conserved pathogen associated molecular patterns (PAMPS) triggered type I interferon (IFN) -mediated innate immune responses. The DNA sensor— cGAS (cGAMP Synthase) recognizes and binds to host or pathogen cytoplasmic DNA, promotes the formation of the second messenger cGAMP (cyclic GMP-AMP), and triggers STING (stimulator of interferon genes) dependent downstream signaling. Here we briefly describe the latest progress of the cGAS-cGAMP-STING pathway and its important role in antivirus, and provide new ideas for virus prevention research and new direction for the development of antiviral drugs.
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Objective To investigate the effects of upadacitinib on the polarization and inflammation of BV2 microglia after oxygen glucose deprivation/recovery (OGD/R) and to explore its mechanism of action. Methods The experiment was divided into 3 groups: control group, OGD group and upadacitinib treatment group. After BV2 cells were treated with OGD/R, MTT was used to detect cell survival rate. Wound scratch assay was used to detect the cell migration ability. qPCR was used to detect mRNA levels of M1-type polarization markers (CD11b, CD32, iNOS) and M2-type polarization markers (Arg-1, IL-10, CD206) of BV2 cells. ELISA was used to detect the levels of IL-1β, IL-6, and TNF-α in the culture medium. Western blot was used to detect the expression levels of JAK1/STAT6 pathway-related proteins. Results Upadacitinib increased the survival of BV2 cells after OGD/R (P<0.05), reduced the polarization of BV2 cells to M1 type (P<0.05). Upadacitinib significantly decreased the migration ability of BV2 cells induced by OGD/R (P<0.05), reduced the inflammatory factors secreted by BV2 cells induced by OGD/R: IL-1β, IL-6, TNF-α (P<0.05). Upadacitinib increased the survival rate of co-cultured PC12 cells (P<0.05). Upadacitinib significantly inhibited the expression levels of p-JAK1 and p-STAT6 proteins in BV2 cells activated by OGD/R induction (P<0.05). Conclusion Upadacitinib decreases polarization of BV2 induced by OGD/R to M1 type and reduces inflammation, which is related to JAK1/STAT6 pathway.
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Tanshinone ⅡA is a kind of phenanthraquinone derivatives derived from Salvia miltiorrhiza,which is one of the main active components of Danshen to play the protective role of cerebral ischemic injury.Inflammation plays an important role in the pathogenesis of cerebral ischemia.In recent years,much evidence shows that immune cells,adhesion molecules,in-flammatory mediators have been involved in the pathogenesis of immune response in the central nervous system through induc-tion or regulation of cerebral ischemia.In this paper,the research progress of mechanism of inflammatory response of tanshi-none ⅡA after cerebral ischemia was reviewed,which provided a new idea for the study of the protective mechanism of tanshi-none ⅡA in cerebral ischemia.
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Objective To study the protective effect of Fu-Yuan-Xing-Nao decoction (FYXND) on rats with middle cere-bral ischemia reperfusion injury .Methods Male Sprague-Dawley rats were randomly divided into sham ,ischemia-reperfusion , and low ,middle ,high FYXND dose (5 .5 ,11 ,22 g/kg) groups .Rats model was induced by 2 h of middle cerebral artery oc-clusion and 24 h reperfusion .The neurological deficit score of each group was evaluated .The infarct size was measured by the 2 ,3 ,5-triphenyltetra-zolium(TTC) chloride staining assay .The pathological changes of brain tissue were observed by HE stai-ning assay .The changes of Nissl bodies were observed by Nissl staining .Tunnel staining was used to observe the apoptosis of neurons in brain .Serum levels of superoxide dismutase (SOD)and Malondialdehyde (MDA ) were measured .Results Com-pared with the model group ,neurological outcomes were improved in all three groups of low ,middle and high FYXND dose (5 .5 ,11 ,22 g/kg) .Significantly reduced infarct brain volume was observed with TTC staining in all three FYXND groups . The results from HE staining assay indicated that the pathological structure of brain tissue was improved in the treatment groups .The numbers and morphology of Nissl corpuscles in the treated group were also improved based on the results of Nissl staining .Both the Tunnel staining positive cells and the rate of apoptosis were decreased .Compared with the model group , FYXND increased the rat serum SOD level and decreased the MDA level .Conclusion FYXND has protective effects on cere-bral ischemia reperfusion injury in rats .
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Traumatic brain injuries(TBI) have caused severe injuries and deaths all over the world ,but so far research-ers have not found an effective drug in treating TBI on clinic .However ,peptides have gradually been in a hot research with its advantages which include safety and tolerance etc .The neuroprotective and anti-inflammatory effects of several peptide com-pounds in traumatic brain injury are reviewed in this paper .
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People do have some risks of exposing to the radiation during their daily life .Longtime or megadose ionizing radiation can induce tissue damage ,which is related to cell apoptosis ,necrosis and inflammation ,etc ..Currently ,more and more radio protective agents were developed and several signaling pathways were involved .NFκB ,MAPK ,PI3k/Akt ,p53 and STAT3 signaling pathways were reviewed in this article .
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Monocyte locomotion inhibitory factor(MLIF)was an anti‐inflammatory pentapeptide produced by Entamoeba histolytica .In vivo and in vitro study showed that MLIF displayed anti‐inflammatory and immune protection effects and MLIF had protective effects on rheumatoid arthritis ,nerve injury ,myocardial ischemia ,cerebral ischemia and Alzheimer′s disease . Studies had shown that MLIF regulated inflammatory response and immune protection through NF‐κB and MAPK signal path‐ways .The sources and biological activities of MLIF were reviewed in this paper .